This invention relates to implantable stimulators generally and more particularly to implantable cardioverters and defibrillators.
Automatic tachycardia detection systems for previously disclosed automatic cardioverter/ defibrillators presently have relied upon the presence or absence of electrical and mechanical heart activity (such as intramyocardial pressure, blood pressure, impedance, stroke volume or heart movement) and/or the rate of the electrocardiogram to detect hemodynamically compromising ventricular tachycardia or fibrillation. Others have suggested the use of physiological sensors such as oxygen saturation sensors to diagnose various types of tachyarrhythmias.
Very generally, the systems that depend upon the aforementioned criteria are capable of discriminating tachycardia in greater or lesser degree from normal heart rate but can have difficulty discriminating ventricular tachycardias from supraventricular tachycardias or in distinguishing sinus tachycardias from non-sinus tachycardias in some circumstances which may result in delivery of inappropriate antitachycardia therapies.
Use of pacing stimuli to discriminate between types of tachyarrhythmias has also been proposed. In the article, "A Single Atrial Extrastimulus Can Distinguish Sinus Tachycardia from 1:1 Paroxysmal Tachycardia" by Jenkins et al, published in Pace, Vol. 9, Part II, Nov.-Dec., 1986, delivery of an atrial premature stimulus is disclosed as a method of distinguishing sinus tachycardia from ventricular tachycardia with one to one retrograde conduction or A-V nodal reentrant tachycardia. This article also discusses various methods of distinguishing among types of tachycardias based upon timing of spontaneous atrial and ventricular contractions.
It is known that stimulation of the vagus nerves can vary the heart's rhythm. This phenomena has often been proposed as a method of treating tachyarrhythmias. It is also known that the nervous system regulating the rhythm of the heart includes a number of highly ganglionated plexi or "fat pads" at various locations on the heart, including fat pads associated with the SA and AV nodes. As set forth in "Functional Anatomy of the Cardiac Efferent Innervation", by Randall et al, in Neurocardiology, edited by Kulbertus et al, Futura Publishing Co., 1988, direct epicardial stimulation of the fat pad associated with the SA node can produce a slowing of the sinus rate and stimulation of the fat pad associated with the AV node can result in a prolongation of the P-R interval or production of A-V block. The effects of stimulation of individual ones of the fat pads are limited to their associated nodes.
As set forth in the article "Neural Effects on Sinus Rate and Atrial Ventricular Conduction Produced by Electrical Stimulation From a Transvenous Electrode Catheter in the Canine Right Pulmonary Artery" by Cooper et al., published in Circulation Research, Vol. 46, No. 1, Jan., 1980, pp. 48-57, the fat pads associated with both the AV node and the sinus node may be stimulated by means of electrodes located in the right pulmonary artery. The results obtained include both a depression of the sinus rate and a prolongation of the A-V conduction time in response to continuous stimulation at 2-80 Hz at up 50 ma.